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DOI 10.1016/j.intimp.2014.11.002

Медицинская библиотека · International immunopharmacology · 2014

Berberine hydrochloride attenuates lipopolysaccharide-induced endometritis in mice by suppressing activation of NF-κB signal pathway.

Fu Kaiqiang, Lv Xiaopei, Li Weishi, Wang Yu, Li Huatao, Tian Wenru, Cao Rongfeng

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Endometritis is a common disease in animal production and influences breeding all over the world. Berberine is one of the main alkaloids isolated from Rhizoma coptidis. Previous reports showed that berberine has anti-inflammatory potential. However, there have been a limited number of published reports on the anti-inflammatory effect of berberine hydrochloride on LPS-induced endometritis. The purpose of the present study was to investigate the effects of berberine hydrochloride on LPS-induced mouse endometritis. Berberine hydrochloride was administered intraperitoneally at 1h before and 12h after LPS induction. Then, a biopsy was performed, and uterine myeloperoxidase (MPO) and nitric oxide (NO) concentrations were determined. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels in the uterus homogenate were measured by ELISA. The extent of IκB-α and P65 phosphorylation was detected by Western blot. The results showed that berberine hydrochloride significantly attenuated neutrophil infiltration, suppressed myeloperoxidase activity and decreased NO, TNF-αand IL-1βproduction. Furthermore, berberine hydrochloride inhibited the phosphorylation of the NF-κB p65 subunit and the degradation of its inhibitor, IκBα. These findings suggest that berberine hydrochloride exerts potent anti-inflammatory effects on LPS-induced mouse endometritis and might be a potential therapeutic agent for endometritis.

Для цитирования: Fu Kaiqiang, Lv Xiaopei, Li Weishi, Wang Yu, Li Huatao, Tian Wenru, Cao Rongfeng. Berberine hydrochloride attenuates lipopolysaccharide-induced endometritis in mice by suppressing activation of NF-κB signal pathway.. International immunopharmacology. 2014. DOI: 10.1016/j.intimp.2014.11.002.

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